SLC4A11 and MFSD3 Gene Expression Changes in Deoxynivalenol Treated IPEC-J2 Cells
Yafei Xu1, Xiaolei Chen1, Luchen Yu1
1Key Laboratory for Animal Genetic, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Frontiers in Genetics
|August 9, 2021
Summary
Deoxynivalenol (DON) causes cell damage, but SLC4A11 and MFSD3 genes can alleviate its toxicity. Increased DNA methylation of these genes correlates with reduced expression and increased DON toxicity in animal cells.
Area of Science:
- Toxicology
- Molecular Biology
- Epigenetics
Background:
- Deoxynivalenol (DON) is a mycotoxin causing significant cytotoxicity in animal cells.
- The molecular mechanisms and regulatory genes involved in DON toxicity are not fully understood.
Purpose of the Study:
- To investigate the role of SLC4A11 and MFSD3 genes in mitigating DON-induced cytotoxicity.
- To analyze DNA methylation changes in SLC4A11 and MFSD3 and their correlation with DON toxicity.
Main Methods:
- Cell viability, cell cycle, and apoptosis assays were performed on IPEC-J2 cells exposed to DON.
- Gene expression levels of SLC4A11 and MFSD3 were analyzed.
- DNA methylation patterns in the promoter regions of SLC4A11 and MFSD3 were assessed using methylation assays.
- Bioinformatic analysis identified transcription factor binding sites.
Main Results:
- DON exposure decreased IPEC-J2 cell viability, arrested the cell cycle at G2/M phase, and increased apoptosis.
- Expression of SLC4A11 and MFSD3 was significantly downregulated by DON.
- Overexpression of SLC4A11 and MFSD3 enhanced cell viability.
- Increased promoter methylation of SLC4A11 and MFSD3 correlated negatively with their mRNA expression.
- Specific methylation sites (mC-1) in SLC4A11 and MFSD3 promoters were located within transcription factor binding sites (NF-1, Sp1).
Conclusions:
- Porcine SLC4A11 and MFSD3 play a crucial role in regulating DON-induced cytotoxicity.
- DNA methylation of SLC4A11 and MFSD3 promoter regions is involved in the modulation of DON toxicity.
- These genes represent potential biomarkers and therapeutic targets for predicting and mitigating DON toxicity.
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